Pulmonary embolism and hemorrhage after displacement of angiographic catheter tip to pulmonary artery: A case report and literature review.

Pulmonary embolism and massive hemoptysis caused by intravascular foreign bodies have rarely been reported. We report a case of an end-stage renal disease patient in which the tip of the angiographic catheter fell off into the pulmonary artery during endovascular interventional opening when the patient underwent vascular access occlusion for dialysis. During the operation, the foreign body was displaced repeatedly and finally anchored to the posterior basal segment branch of the right lower pulmonary artery. A pulmonary embolism occurred during the operation, and massive hemoptysis and hemorrhagic shock occurred after anticoagulation and thrombolytic therapy. After receiving anti-shock and symptomatic treatment, the patient gradually recovered. After six months of follow-up, no pulmonary embolism or pulmonary infarction occurred. Our case report presents an alternative approach to extracting a foreign object from the pulmonary artery by locating the foreign object within the vascular terminations, without resorting to forceful removal. This method mitigates the potential risks of pulmonary embolism and bleeding associated with forceful extraction.

Imaging misdiagnosis and clinical analysis of significant hepatic atrophy after bilioenteric anastomosis: A case report.

BACKGROUND: The occurrence of long-term bilioenteric anastomotic stenosis can readily induce liver atrophy and hyperplasia, thereby causing significant alterations in the anatomical and morphological aspects of the liver. This condition significantly hampers the accuracy of preoperative imaging diagnosis, while also exacerbating the complexity of surgical procedures and the likelihood of complications. CASE SUMMARY: A 60-year-old female patient was admitted to the hospital presenting with recurring epigastric pain accompanied by a high fever. The patient had a history of cholecystectomy, although the surgical records were not accessible. Based on preoperative imaging and laboratory examination, the initial diagnosis indicated the presence of intrahepatic calculi, abnormal right liver morphology, and acute cholangitis. However, during the surgical procedure, it was observed that both the left and right liver lobes exhibited evident atrophy and thinness. Additionally, there was a noticeable increase in the volume of the hepatic caudate lobe, and the original bilioenteric anastomosis was narrowed. The anastomosis underwent enlargement subsequent to hepatectomy. As a consequence of the presence of remaining stones in the caudate lobe, the second stage was effectively executed utilizing ultrasound-guided percutaneous transhepatic catheter drainage. Following the puncture, three days elapsed before the drain tip inadvertently perforated the liver, leading to the development of biliary panperitonitis, subsequently followed by pulmonary infection. The patient and her family strongly refused operation, and she died. CONCLUSION: The hepatic atrophy-hypertrophy complex induces notable alterations in the anatomical structure, thereby posing a substantial challenge in terms of imaging diagnosis and surgical procedures. Additionally, the long-term presence of hepatic fibrosis changes heightens the likelihood of complications arising from puncture procedures.

Wernicke's encephalopathy after acute pancreatitis with upper gastrointestinal obstruction: A case report and literature review.

A 42-year-old female was admitted with upper abdominal pain. Imaging studies and laboratory tests were performed to consider acute lipogenic pancreatitis. After symptomatic treatment, her abdominal pain was significantly relieved. However, the patient was accompanied by upper gastrointestinal obstruction, which was gradually relieved after long-term fasting, gastrointestinal decompression, and fluid rehydration. The patient developed dizziness and ataxia, which worsened. Cranial magnetic resonance imaging (MRI) indicated patchy abnormal signal shadows in the bilateral thalami and dorsal brainstem and suggested metabolic encephalopathy. Wernicke's encephalopathy (WE) was the initial diagnosis of suspicion, adequate vitamin B1 was immediately replenished until the complete resolution of symptoms, and the patient made a rapid and dramatic recovery.

Control system of neoclassical tearing modes in real time on HL-2A tokamak.

The stability and performance of tokamak plasmas are routinely limited by various magneto-hydrodynamic instabilities, such as neoclassical tearing modes (NTMs). This paper presents a rather simple method to control the NTMs in real time (RT) on a tokamak, including the control principle of a feedback approach for RT suppression and stabilization for the NTMs. The control system combines Mirnov, electron cyclotron emission, and soft X-ray diagnostics used for determining the NTM positions. A methodology for fast detection of 2/1 or 3/2 NTM positions with 129 × 129 grid reconstruction is elucidated. The forty poloidal angles for steering the electron cyclotron resonance heating (ECRH)/electron cyclotron current drive launcher are used to establish the alignment of antenna mirrors with the center of the NTM and to ensure launcher emission intersecting with the rational surface of a magnetic island. Pilot experiments demonstrate the RT control capability to trace the conventional tearing modes (CTMs) in the HL-2A tokamak. The 2/1 CTMs have been suppressed or stabilized by the ECRH power deposition on site or with the steerable launcher.

Augmenter of liver regeneration attenuates acute rejection after rat liver transplantation.

BACKGROUND: The role of augmenter of liver regeneration (ALR) on liver transplantation immune regulation remains unknown. METHODS: Male Lewis and Brown-Norway (BN) rats were assigned to allograft group (Lewis-to-BN liver transplantation), isograft group (BN-to-BN), and ALR group (Lewis-to-BN, ALR, 100 µg/kg/d, intramuscular injection postoperatively). Rats were sacrificed at indicated times for assessment of cytokines production, T-cell (TC) activation and apoptosis. Kupffer cells (KCs) and TCs were isolated from grafts to assess cytokine expression. Effect of ALR and KCs on TCs was monitored by co-culture of (3)H-thymidine TCs. RESULTS: (1) Treatment with ALR significantly decreased interleukin-2 and interferon-γ expression, promoted TC apoptosis, and prolonged the survival of allografts; (2) KCs in ALR group and isograft group that had significantly increased interleukin-10 and decreased tumor necrosis factor-α expression were able to inhibit TC proliferation and induce their apoptosis relative to KCs in the allograft group; (3) ALR and KCs directly inhibited TC proliferation and activation and induced TC apoptosis. CONCLUSIONS: ALR could inhibit TC proliferation and function both in vivo and in vitro and attenuate acute rejection after liver transplantation.

Development of a low-drift integrator system on the HL-2A tokamak.

In this work, we developed a new integrator system with low-drift and small integration time constant less than 1 ms, which applies to the weak signals from magnetic measurements. This integrator system is designed on the basis of the analog drift compensation and the real-time digital correction of residual drift. The analog drift compensation is achieved by the subtraction between two integrators and the digital correction method is available due to the stability of integral drift in short time scale. The algorithm of the residual drift calculation and correction is implemented by the field programmable gate array. The integral drift can be well compensated within 10 mV/10 s at RC = 0.5 ms and meet the requirements of magnetic diagnostic on HL-2A.

Traumatic diaphragmatic rupture with combined thoracoabdominal injuries: Difference between penetrating and blunt injuries.

PURPOSE: Traumatic diaphragmatic rupture (TDR) needs early diagnosis and operation. However, the early diagnosis is usually difficult, especially in the patients without diaphragmatic hernia. The objective of this study was to explore the early diagnosis and treatment of TDR. METHODS: Data of 256 patients with TDR treated in our department between 1994 and 2013 were analyzed retrospectively regarding to the diagnostic methods, percentage of preoperative judgment, incidence of diaphragmatic hernia, surgical procedures and outcome, etc. Two groups were set up according to the mechanism of injury (blunt or penetrating). RESULTS: Of 256 patients with a mean age of 32.4 years (9-84), 218 were male. The average ISS was 26.9 (13-66); and shock rate was 62.9%. There were 104 blunt injuries and 152 penetrating injuries. Preoperatively diagnostic rate was 90.4% in blunt injuries and 80.3% in penetrating, respectively, P < 0.05. The incidence of diaphragmatic hernia was 94.2% in blunt and 15.1% in penetrating respectively, P < 0.005. Thoracotomy was performed in 62 cases, laparotomy in 153, thoracotomy plus laparotomy in 29, and combined thoraco-laparotomy in 12. Overall mortality rate was 12.5% with the average ISS of 41.8; and it was 21.2% in blunt injuries and 6.6% in penetrating, respectively, P < 0.005. The main causes of death were hemorrhage and sepsis. CONCLUSIONS: Diagnosis of blunt TDR can be easily obtained by radiograph or helical CT scan signs of diaphragmatic hernia. For penetrating TDR without hernia, "offside sign" is helpful as initial assessment. CT scan with coronal/sagittal reconstruction is an accurate technique for diagnosis. All TDR require operation. Penetrating injury has a relatively better prognosis.

Knockdown of microRNA-155 in Kupffer cells results in immunosuppressive effects and prolongs survival of mouse liver allografts.

BACKGROUND: Our previous studies have shown that Kupffer cells (KCs) play a crucial role in postoperative pathologic changes. Recent reports have demonstrated that microRNA-155 (miR-155) is associated with inflammation and upregulation of proinflammatory mediators in the peripheral blood and allografts of transplant patients. However, the precise mechanism for this remains unknown. METHODS: KCs isolated from BALB/c mice were transfected with miR-155 mimic or inhibitor. Levels of suppressor of cytokine signaling 1/Janus kinase/signal transducer and activator of transcription (SOCS1/JAK/STAT) proteins and surface molecules (MHC-II, CD40, and CD86) were then measured. T-cell proliferation and apoptosis were evaluated in mixed lymphocyte reactions. Orthotopic liver transplantation was performed in mice after miR-155 short hairpin RNA lentivirus treatment, and postoperative survival, liver function and histology, and mRNA and protein expression were analyzed. RESULTS: miR-155 knockdown in KCs decreased MHC-II, CD40, and CD86 expression, suppressed antigen-presenting function, and affected SOCS1/JAK/STAT inflammatory pathways. In addition, KCs transfected with miR-155 inhibitor and cocultured with T lymphocytes showed reduced T-cell responses but a greater number of apoptotic T cells. Finally, miR-155 suppression in graft liver prolonged liver allograft survival and improved liver function. The changes were closely associated with the levels of T helper 1 and 2 (Th1/Th2) cytokines and T-cell apoptosis, but a direct mechanistic link in vivo was not established. CONCLUSION: These data suggest miR-155 regulates the balance of Th1/Th2 cytokines and the maturation and function of KCs in mice. miR-155 repression in KCs positively regulates KC function toward immunosuppression and prolongs liver allograft survival.

Correlation between augmenter of liver regeneration and IFN-γ expression in graft after rat orthotopic liver transplantation.

BACKGROUND: Previous data suggested that augmenter of liver regeneration (ALR) has immunomodulation function by suppressing liver-resident NK cell activity and reducing IFN-γ expression in human liver diseases. The correlation between ALR and IFN-γ expression in graft after rat orthotopic liver transplantation remains uncertain. METHODS: A Lewis-to-BN (allograft group) and BN-to-BN (isograft group) rat liver transplantation model was used to investigate the ALR and IFN-γ expression in liver graft. Graft recipients were sacrificed at days 1, 3, 5, and 7 posttransplantation. The histopathologic changes of grafts were observed under light microscope and the intragraft expression of ALR and IFN-γ mRNA and protein was determined by real-time PCR and immunohistochemistry staining, respectively. Correlation between ALR and IFN-γ expression in graft was evaluated by Spearman rank correlation analysis. RESULTS: The light microscope inspection revealed severe acute rejection in the allograft group but not in the isograft group at day 7 after liver transplantation. The intragraft ALR showed slight protein expression at day 1 after liver transplantation in both groups and it was significantly increased at days 3, 5, and 7 (P < 0.05). There was no significant difference in ALR mRNA expression between the allograft group and isograft group at day 1 (1.09 ± 0.12 and 1.13 ± 0.10, respectively; P > 0.05, n = 3). The ALR mRNA level was slightly reduced at day 3 in both groups compared with that at day 1 (0.81 ± 0.11 and 0.59 ± 0.10, respectively, P > 0.05). However, it was markedly increased at day 5 (2.86 ± 0.37) and day 7 (3.19 ± 0.33) in the isograft group and was 1.57 ± 0.27 and 1.98 ± 0.13 in the allograft group at days 5 and 7, respectively. IFN-γ protein and mRNA expression in the allograft group was increased at day 1 posttransplantation and reached a peak at day 3, and then it had a slight tendency of decline at day 5 and day 7. And they in the isograft group were at a low level at all times. The levels of ALR mRNA showed a negative correlation with levels of IFN-γ mRNA in the allograft group (r = -0.86, P < 0.05, y = -0.241x + 0.586), whereas there is no correlation between ALR and IFN-γ mRNA expression in the isograft group. CONCLUSION: These data revealed an obviously negative correlation between ALR and IFN-γ levels intragraft, which indicated that ALR may participate in immunoregulation of acute rejection.

Effect of taurine on IRAK4 and NF-kappa B in Kupffer cells from rat liver grafts after ischemia-reperfusion injury.

BACKGROUND: The aim of this study was to explore the protective mechanisms of taurine pretreatment against hepatic ischemia/reperfusion injury after liver transplantation. METHODS: A Sprague-Dawley-to-Sprague-Dawley rat liver transplantation model was used in this study. At 0, 60, and 180 minutes after reperfusion, expression of interleukin-1 receptor-associated kinase-4 (IRAK-4) messenger ribonucleic acid and protein in Kupffer cells was determined by real-time polymerase chain reaction and Western blotting. The activity of nuclear factor κB in Kupffer cells was determined by electrophoretic mobility shift assay. The serum tumor necrosis factor-α level was detected by enzyme-linked immunosorbent assay. Serum transaminases, liver histology, and animal survival were also investigated. RESULTS: At 60 and 180 minutes after reperfusion, levels of IRAK-4 messenger ribonucleic acid and protein, activities of nuclear factor κB, and levels of serum transaminases and tumor necrosis factor-α were all obviously elevated. However, changes in these parameters in rats treated with taurine were remarkably attenuated at the indicated time points. CONCLUSIONS: These data suggest that taurine could protect against hepatic ischemia/reperfusion injury after liver transplantation, and the protective effects may be through downregulation of IRAK-4 and downstream nuclear factor κB and tumor necrosis factor-α expression in Kupffer cells.

Protective effect of glutamine-enriched early enteral nutrition on intestinal mucosal barrier injury after liver transplantation in rats.

BACKGROUND: The effect of glutamine-enriched early enteral nutrition (Gln-EEN) on intestinal mucosal barrier injury after liver transplantation (LT) remains uncertain. METHODS: The Wistar-to-Wistar rat LT model was used to explore the protective effect of Gln-EEN. Morphologic changes of intestinal mucosa, levels of intestinal malondialdehyde and secretory immunoglobulin (sIgA), plasma endotoxin, D-lactic acid, serum tumor necrosis factor-alpha (TNF-alpha), rates of bacterial translocation, and expression of intestinal nuclear factor-kappaB, TNF-alpha, and intercellular adhesion molecule-1 were determined. RESULTS: After LT, intestinal mucosa was damaged seriously. At 12, 24, and 48 hours posttransplantation, levels of intestinal sIgA were decreased; levels of malondialdehyde, endotoxin, D-lactic acid, and TNF-alpha, the ratio of bacterial translocation, and the expression of intestinal nuclear factor-kappaB, TNF-alpha, and intercellular adhesion molecule-1 all were increased. However, changes in earlier-mentioned parameters in recipients treated with Gln-EEN were attenuated remarkably at 24 to 48 hours. CONCLUSIONS: Our data show that Gln-EEN is a potent protectant against intestinal mucosal barrier injury after LT.

Knockdown of interleukin-2 by shRNA-mediated RNA interference prolongs liver allograft survival.

Interleukin-2 (IL-2) plays a central role in T-cell activation, expansion, and homeostasis. The failure of IL-2 biosynthesis may play a critical role in tolerance induction. We tested the effect of IL-2 blockade by short hairpin RNA (shRNA) on regulating acute rejection in rat liver transplantation. To this end, we successfully designed and selected an effective interference plasmid, pIL-2B. The IL-2 mRNA expression level in the pIL-2B group was one-fifth of that in the no transfection group. Lewis to BN orthotopic liver transplant model was used to explore the effect of knockdown IL-2 by shRNA in vivo. Recipients treated with pIL-2-shRNA survived longer (median survival time of 16 d range 7-21 d) than those with empty vector (11; range 5-13) or saline (9; range 5-13) (P<0.05), and was inferior to those with CsA (24; range 13-36, P<0.05). The IL-2-shRNA attenuated acute rejection with decreased apoptosis of hepatocytes and reduced cytokine production of IL-2, tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma) in the graft. Our results suggest that IL-2 targeting using RNA interference approach may be of potential interest in organ transplantation.

Blockade of inducible costimulator pathway to prevent acute rejection in rat liver transplantation.

BACKGROUND: The role of inducible costimulator (ICOS) in transplantation immunity remains unclear. METHODS: A Lewis-to-Brown-Norway (BN) rat liver transplant model was used to explore the effect of ICOS blockade by small interference RNA. Recipient survival rate, number of CD25/ICOS-positive cells, ICOS mRNA and protein levels, and interferon-gamma and tumor-necrosis factor-alpha levels were determined. RESULTS: Recipient survival was significantly prolonged in rats treated with RNA interference. On day 7 after transplantation, there was a diminished frequency of CD25/ICOS-positive cells and an increased frequency of apoptotic T cells. Furthermore, we found that ICOS blockade could inhibit mRNA and protein expression of ICOS, decrease plasma levels of interferon-gamma and tumor-necrosis factor-alpha, suppress cell infiltration into grafts, and promote tolerance in the interference group. CONCLUSIONS: Our data demonstrate that RNA interference is a potent tool to down-modulate ICOS expression and protect allografts from acute rejection.

Role of Kupffer cells in the induction of tolerance of orthotopic liver transplantation in rats.

Because the role of Kupffer cells (KCs) in liver transplantation (LT) tolerance is not well understood, we investigated their role in liver allograft acceptance in rats. Male Sprague-Dawley rats were randomly assigned to either an LT group or a transplantation group pretreated with GdCl(3) (Gd group). The rats were postoperatively sacrificed at indicated times for histology and assessment of KC function, nuclear factor kappa B (NF-kappaB) activity, and cytokine production. KCs and T cells (TCs) were isolated from allografts to assess Fas/Fas ligand (FasL) expression. Cytotoxicity of KCs against TCs was monitored by coculturing of (3)H-thymidine TCs with KCs at various effector-to-target ratios. The results were as follows. First, grafts were spontaneously accepted in the LT group with evident apoptosis of TCs; however, inhibition of KCs by pretreatment with GdCl(3) decreased TC apoptosis and shortened the survival of allografts. Second, KCs in the LT group had increased levels of FasL messenger RNA and protein with respect to that in the Gd group. Third, by in vitro cocultivation assays, KCs induced TC apoptosis though elevated expression of FasL, and this process could be blocked by anti-FasL antibody. Fourth, there was a positive correlation between activation of NF-kappaB and FasL expression in KCs and interleukin-4 production in the LT group, and the activation of NF-kappaB was inhibited by pretreatment with GdCl(3). In conclusion, KC-induced depletion of TCs via the Fas/FasL pathway might play a critical role in LT tolerance. However, the tolerance is abrogated by suppression of FasL and IL-4 expression via inhibition of NF-kappaB activity by GdCl(3).